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Clinical Characteristics

As has already been noted, there are many factors which affect the complicated life cycle and behavior of the schistosome. This is also true of the clinical manifestations. At every stage in the cycle of invasion and maturation there is some clinical reaction: it varies with the individual, with the immune status, with the parasitic load, with the species of schistosome, and with many other factors, which include the patient's age and general state of nutrition and health, as well as the presence of other schistosomes or parasites. Previous infection only provides a limited protection. Chimpanzees can be successfully immunized, but so far (2000) there is no tested human vaccine. Reinfection may produce an illness differing from the primary infection, and the nature of that reaction may depend on whether or not the patient is currently infected.

Clinical Summary

The clinical findings in schistosomiasis can be summarized as follows:

1. During the acute phase of infestation: urticaria, pruritus, cough, fever and eosinophilia: abdominal pain and less commonly, CNS symptoms.

2. After a few months, general debility, ill health and anemia, headaches.

3. At the stage of oviposition: hematuria or bloody stools with dysentery.

4. There may be side effects, such as persistent and severe Salmonella infections or increased miscarriages and stillbirths. Hepatitis B infections may also be more frequent and severe.

5. Finally, portal cirrhosis, esophageal varices, hemorrhoids, pulmonary fibrosis and hypertension, urinary infection, carcinoma of the bladder, or chronic rectal bleeding with rectal prolapse, anemia and infections.

Many of these changes will be irreversible. During the acute phase the administration of steroids may reduce the permanent effects: even the hypersplenism may subside, but once the granulomas are established it is difficult to prevent their progress. Surgery may be required to relieve urinary obstruction, to manage portal hypertension and to deal with the effects on the bowel. Urinary schistosomiasis is associated with an increased incidence of bladder carcinoma (a complex etiological relationship) and there is an increased incidence of bowel cancer in patients with S. japonicum infections. Whether S. mansoni or S. haematobium cause increased cancer of the colon is still controversial. There is no evidence linking schistosomiasis with cancer of the lung.


Katayama Syndrome

The acute stage of infection with any of the schistosomes is known as the "Katayama syndrome." This name was originally given to an urticarial fever in China, which in about 1907 was recognized to be the result of early infection with S. japonicum. Later the syndrome was seen in early schistosomiasis caused by any schistosome. It follows exposure to infected water about 3-9 weeks previously. The majority of patients who exhibit this syndrome will not have been previously infected by schistosomes and the syndrome may therefore be seen in travelers returning from endemic areas. For example, six out of seven American tourists exposed to river water in west Africa were ill within 4 weeks and became seropositive for S. mansoni. The Katayama syndrome is similar to serum sickness, an antibody-antigen reaction with raised IgE and IgG. It can be life threatening. Eggs will eventually be found in the urine or feces between 40 and 50 days after the contact, but may take over 90 days to appear, by which time the "Katayama" stage may be long past.

At the stage of exposure to the cercaria, many patients will exhibit no clinical reaction and have no complaints. Indigenous populations in particular seldom develop cercarial dermatitis. In the nonsensitized, there may be burning and irritation of the skin (swimmer's itch) followed in some cases by urticaria within the first 24 or 48 hours. This may have no clinical significance, being due to avian or animal cercaria. In fact, some authorities distinguish the clinical appearance of a cercarial dermatitis, which is a maculopapular rash which can last about 2-3 weeks and is not due to human schistosomiasis, and restrict the term "schistosomal dermatitis" to the short- lived specific itchy, papular rash which results from contact with human schistosomes. In everyday practice, however, the history of an itchy rash or transient sunburn, with ill health after contact with fresh water in the tropics, is significant and important. About 25%of patients will feel tired and "off color". These complaints may have no clinical significance, being due to animal cercaria. If the infection has been massive, there may be very severe skin irritation and the condition may be mistaken for sunburn or other skin allergy.

This is followed by a latent period, which usually lasts from 3-9 weeks and then the patient may complain of headache, backache, chills, fever, night sweats, nonproductive cough, abdominal discomfort, and profound anorexia and distaste for food. The temperature will vary from 99° to 105°F ( 37.2° - 40.6°C). Urticaria and/or diarrhea occur in 25% of patients. This probably coincides with the stage of migration of the larvae through the blood vessels and can be associated with radiological changes in the chest and elsewhere. The most constant finding on examination of the blood is eosinophilia, which frequently may reach between 15% and 50%; in a few cases it can reach 90% or 20,000 eosinophils per mm³. Again, individual variation is considerable and patients may be asymptomatic or moderately or extremely ill. When the acute infection is massive in a patient not previously exposed to any schistosomes, the resulting illness can be serious and life threatening. Headache and neck stiffness may be severe, tenderness can develop over the liver, and the cough can be extremely troublesome.The serological tests should be positive, but a negative test at this stage does not exclude schistosomiasis.

For all species of schistosomes, the acute abdominal symptoms probably represent the invasion of the hepatic and portal veins, the mesenteric vessels and lymphatics. Thereafter, the symptoms are related more specifically to the eggs than to the worms. The passage of eggs through the intestinal wall will be accompanied by diarrhea, with mucus and extravasated blood. Other embolic ova lodge in the small intestine, appendix, heart (cardiac arrhythmia can develop), pancreas, kidneys, adrenals, ovaries, fallopian tubes, lymph nodes, retroperitoneal tissues and omentum. Especially in S. japonicum infections, the embolic eggs may become lodged in the brain and may cause an acute encephalitis, with loss of consciousness and extensor plantar responses; the EEG may be abnormal. In some patients there have been transitory paralysis, visual impairment, incontinence, ataxia and even seizures and coma.Wherever they lodge, all eggs may cause a local a cellular or granulomatous reaction.

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Copyright: Palmer and Reeder